In strains of the snail Biomphalaria glabrata (Gastropoda) that are resistant to the parasite Schistosoma mansoni (Trematoda), hemocytes in the hemolymph are responsible for elimination of S. mansoni sporocysts. The defensive role of reactive nitrogen species was investigated in in vitro interactions between hemocytes derived from the resistant 13-16-R1 strain of B. glabrata and the parasite. The nitric oxide synthase (NOS) inhibitor Nω-nitro-l-arginine methylester (l-NAME) and the nitric oxide (NO·) scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide reduced cell-mediated killing of S. mansoni sporocysts. To determine if peroxynitrite (ONOO) is involved in killing, assays were run in the presence of the ONOO scavengers uric acid and deferoxamine. These did not influence the rate of parasite killing, indicating that NO· is directly responsible for mediating cytotoxicity, but ONOO is not. The combination of the NOS inhibitor l-NAME and catalase, an enzyme that detoxifies hydrogen peroxide (H2O2), reduced average sporocyst mortality to a greater extent than l-NAME alone. Killing of the sporocysts was, however, not totally inhibited. It is suggested that NO· and H2O2 are both involved in hemocyte-mediated toxicity of 13-16-R1 B. glabrata against S. mansoni sporocysts.

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